APPENDIX I-S:  Crinnion, Environmental Medicine, Part 4:

Pesticides – Biologically Persistent and Ubiquitous Toxins, Page 432 Alternative Medicine Review _ Volume 5 Number 5 _ 2000




This appendix is copied from:


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Environmental Medicine, Part 4:

Pesticides – Biologically Persistent and

Ubiquitous Toxins.

Walter J. Crinnion, ND


Although the use of pesticides has doubled every ten years since 1945, pest damage

to crops is more prevalent now than it was then. Many pests are now pesticide resistant

due to the ubiquitous presence of pesticides in our environment. Chlorinated pesticide

residues are present in the air, soil, and water, with a concomitant presence in humans.

Organophosphate and carbamate pesticides—the compounds comprising the bulk of

current pesticide use—are carried around the globe on air currents. Municipalities,

schools, churches, business offices, apartment buildings, grocery stores, and

homeowners use pesticides on a regular basis. Pesticides are neurotoxins that can

cause acute symptoms as well as chronic effects from repeated low-dose exposure.

These compounds can also adversely affect the immune system, causing cell-mediated

immune deficiency, allergy, and autoimmune states. Certain cancers are also associated

with pesticide exposure. Multiple endocrine effects, which can alter reproduction and

stress-handling capacity, can also be found. Limited testing is available to assess the

toxic overload of these compounds, including serum pesticide levels and immune system

parameters. Treatment for acute or chronic effects of these toxins includes avoidance,

supplementation, and possibly cleansing.

( Altern Med Rev 2000;5(5)432-447)


The objective of pesticide use to prevent crop loss from insects remains unachieved. K.

Ausubel in his book, Seeds of Change, The Living Treasure, notes that since 1945 overall pesticide

use has risen 3,300 percent, while overall crop loss due to insects has risen 20 percent in the

same time period.1 Ausubel reminds us about Martin Borlaug and the “Green Revolution,”

which introduced F1 hybrid seeds that provided exceptional crop yield when augmented by

utilizing high nitrogen fertilizer. To protect plant growth, herbicides were needed to prevent

weeds from competing for nutrients and space, as well as pesticides to prevent pest-induced

crop damage.

The killing of primary pests with pesticides has paved the way for secondary pests to

come to the fore. Where previously there were 10 primary pest insects – defined as causing

greater than one million dollars of crop damage per year – there are now 300. Of the 25 most

serious pests, 24 were previously secondary pests and 72 percent of these are now pesticide


Walter Crinnion, ND – Healing Naturally, 11811 NE 128th St, Ste 202, Kirkland, WA 98034.

Copyright©2001 Thorne Research, Inc. All Rights Reserved. No Reprint Without Written Permission


Alternative Medicine Review _ Volume 5, Number 5 _ 2000 Page 433

Non-Occupational Pesticide


Of the 2.5 million tons of pesticides

used worldwide each year, less than 0.1 percent

reaches the target pest.2,3 Thus, 99+ percent

of currently applied pesticides are being

released indiscriminately into the environment,

many of which will persist for years and travel

far from the point of application.

Chlorinated pesticides found in the soil

can persist for decades. Dichlorodiphenyltrichloroethane

(DDT- see Figure 1) has

been shown to accumulate in soils where it

was used agriculturally.4 Soil-based DDT is

incorporated into grasses growing in the soil,

into cattle consuming the grass, and eventually

into the milk and fat tissue of the cows.5

While the half-life of DDT had been thought

to range between 4-30 years, evidence from

the Yakima River drainage in Washington

State, and in other areas, points to a much more

extended half-life.6 The studies in this area

show increased levels of p,p’-DDT in the soil

and the persistence of ratios of p,p’-DDT: o,p’-

DDT found in the parent compound applied

25 or more years earlier. This indicates that in

certain soils DDT degradation is not occurring

as rapidly as previously thought.

Such persistence has been found in

other areas of the United States, such as soil

in Texas and New Mexico.7 When soil previously

used agriculturally is excavated to accommodate

housing sites, DDT finds its way

into nearby streams and rivers via erosive runoff.

The study of the Yakima River drainage

found DDT in 100 percent of the fish sampled

from that river. Other rivers, such as the South

Platte, show a multitude of organochlorine

pesticides in both sediment and fish.8

When houses are built on previously

contaminated land, pesticides can easily be

brought from the soil (from residents merely

being “outside,” from working in the garden,

etc.) into the house, where they contaminate

the home as house dust, as previously shown

to do.9 Pesticide exposure via house dust has

been shown to cause higher serum levels of

pesticides than what is incurred by eating contaminated

foods.10 There is also the possibility

of pesticide contamination of vegetables

grown in the home garden.

Those compounds not trapped in soil,

tree bark, sediment, animals, humans, or other

stable material begin a wind-driven leapfrogging

around the globe.11 Volatile chemicals

move more frequently whenever the ambient

temperature is sufficient to volatilize them.

Less volatile compounds, like DDT, stay in

place longer before being volatilized again.

Residues of DDT and other halogenated

compounds have been found in medicinal

herbs picked in the forests of Poland and

Germany, where no spraying of DDT in these

areas has been reported.12,13 In a Polish study,

herbs from all regions of the country were

found to contain pesticide residues. The authors

concluded, “Pesticide contents in most

of the herbal raw materials should be attributed

to the global contamination of the environment.”

When these compounds reach upper

latitudes and colder temperatures, they precipitate

from the air and tend to stay trapped in

whatever material they settle in. This has led

to high amounts being found in the mountains

of Western Canada,14 the Arctic Ocean,16 and

recently even Aleutian eagles’ eggs.16 It likely

accounts for the high amounts of toxins found

in breast milk of indigenous Inuit mothers subsisting

on traditional diets.17 Decades of precipitation

of airborne chlorinated pesticides in

the Arctic have resulted in fat accumulation

of these residues throughout the food chain,

ultimately being transferred to Inuit infants

through breast milk.

Fortunately, 120 countries currently

participating in the United Nations Environmental

Programme are negotiating agreements

for global action on the movement of pesticides

and other chemical pollutants from one

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country to another.18 It is hoped such agreements

will lead to lower levels of airborne traveling

toxins. Unfortunately, this effort does not

address current pesticide loads found in every

part of the planet.

Pesticides of every category have been

found in groundwater throughout the United

States. The U.S. Geological Survey’s analysis

of groundwater found pesticides in the water

from agricultural areas,19 and large amounts

of pesticides have also been found in urban

waterways, primarily due to frequent overapplication

by homeowners. The Mercer

Slough, a protected wetlands area in Bellevue,

Washington, has been found to contain 18 different

types of pesticides.20 Pesticide residues

are also found in foods; the 12 most contaminated

fruits and vegetables being strawberries,

bell peppers, spinach, cherries (U.S.), peaches,

cantaloupe (Mexican), celery, apples, apricots,

green beans, grapes (Chilean), and cucumbers.

The choice exists, of course, to either

find alternative, less-contaminated fruits and

vegetables, or purchase organic varieties of

these items; however, given existing global

pollution levels, food labeled “organically

raised” does not necessarily mean “pesticidefree.”

Foods grown without pesticides can absorb

pesticides from the soil, or be exposed to

them in the air while growing, or during packing

and transportation. Some foods, such as

squash and carrots, may actually concentrate

chlorinated compounds from the soil while


While adults can make an informed

choice about what foods to eat, infants cannot.

While there are numerous beneficial aspects

of breastfeeding, numerous studies have

shown persistent chlorinated pesticide residues

in breast milk. This startling fact has been recorded

in tests of breast milk around the globe,

including South Africa,21,22 Kenya,23 Saudi

Arabia,24 Jordan,25 Sweden,26 Finland,27 Turkey,

28 Poland,29 Ukraine,30 Germany,31 Hong

Kong,32 Australia,33 New Guinea,34 Mexico,35-

37 Brazil,38 Canada,39,40 and Arkansas41 and

New York42 in the United States. DDT residues

(including DDT, DDE

[Dichlorodiphenyldichloroethylene] and DDD

[dichlorodiphenyldichloroethane]) have been

found in 93-100 percent of the milk samples

in these studies.

High levels of polychlorinated biphenyls

(PCB) and hexachlorocyclohexanes

(HCH) – also referred to as BHC – are also

frequently found. The majority of these studies

also found numerous other chlorinated

compounds, including hexachlorobenzene

(HCB), endrin, dieldrin, and various


Most contaminated breast milk

samples have a combination of many such

compounds. All studies had samples that exceeded

the World Health Organization’s acceptable

daily intake of 0.005 mg/kg/day. Levels

of these compounds in breast milk were

shown to correlate directly with the level of

such compounds in maternal adipose tissue.

Furthermore, infant serum levels of pesticides

were shown to correlate with maternal breast

milk levels, and not with airborne exposure.

Pesticide levels in the milk and adipose tissue

of mothers decreased with each breast-fed


Maternal pesticide exposures from diet

or airborne sources have been associated with

maternal load. However, a study in Papua, New

Guinea, was conducted in an area where there

had been no DDT use, yet all lactating women

had DDT in their breast milk. This was most

likely due to the previously discussed movement

of DDT on global air currents. Since

pesticides can bioaccumulate over decades,

and can be passed to the next generation

through both cord blood and breast milk,23 the

implication is that each succeeding generation

begins life with a pesticide load it took their

parents decades to develop.

Children can also be exposed to organophosphate

pesticides (OP), such as

chlorpyrifos, from home use of this compound.

It was demonstrated that after a single broadPesticides

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cast in apartment rooms of this pesticide by

certified applicators (not the typical homeowner),

chlorpyrifos continued to accumulate

on children’s toys and hard surfaces for two

weeks after spraying.43 Based on this and similar

studies it was estimated that after indoor

spraying, children were exposed to levels from

21-119 times the current reference dose of 3


From these and others studies that

found birth defects associated with

chlorpyrifos,45 the U.S. Environmental Protection

Agency recently banned home use of this

compound and imposed tighter restrictions on

the pesticide’s use on some agricultural products,

specifically apples and grapes, and

banned its use on tomatoes. These restrictions

are designed to eliminate the chemical’s residues

on foods often consumed by children. The

pesticide may still be used on a variety of

grains and other crops; however, retail sale will

be stopped after December 31, 2001. Despite

overwhelming scientific evidence, no recall of

existing stock was issued.

Pesticide Presence in Human

Adipose Samples

Studies examining general populations

for chlorinated pesticide residues have found

the presence of multiple chlorinated hydrocarbons

(DDT, DDE, DDD, aldrin, dieldrin, heptachlor,

heptachlor epoxide, and PCBs) in the

adipose tissue of residents of Greenland and

Denmark.46 Adipose samples from women in

Germany, The Netherlands, Northern Ireland,

Spain, and Switzerland, as part of the European

Study on Antioxidants, Myocardial Infarction

and Cancer of the Breast, showed the

consistent presence of DDE.47

An adipose study of 40 autopsied

trauma victims in Israel revealed DDE in all

40, HCB in 34, beta hexachlorocyclohexane

in 27, DDT in seven, and gamma HCH in two.

Three or more chlorinated residues were found

in 80 percent of all studied.48

Samples of adipose tissue and other

fluids taken from 17 caesarean section deliveries

in Germany and Tanzania revealed chlorinated

residues in all women. Those from

Germany had higher levels of HCB and PCBs,

while those from Tanzania had higher levels

of DDT and DDE.49 This study found maternal

adipose tissue contained a 10 to 100-fold

increase in accumulation of chlorinated hydrocarbons

compared to other tissues and fluids

tested. The concentration of certain toxins was

higher in fetal cord blood and the placenta than

in the maternal serum. These persistent chlorinated

pesticide residues have also been found

in adipose tissue throughout North and South


The above-mentioned studies all investigated

biologically persistent chlorinated hydrocarbons.

Such tests for determining the

presence of the non-biologically-persistent

organophosphate, carbamate, and pyrethroid

pesticides are not available, although the metabolite

of chlorpyrifos, one of the most common

organophosphates, was found in the urine

of 82 percent of U.S. adults.55 However, these

studies provide a clear indication that more

than the toxic effect of a single pesticide must

be considered. Based on the above-mentioned

studies, the average person, wherever they live

in the world, most likely has more than one

chlorinated hydrocarbon residue in their adipose

and serum components. To this load can

be added any of the organophosphate, carbamate,

pyrethroids, or arsenical pesticides that

may be in the air, food, or water, as well as

solvents, heavy metals, polycyclic aromatic

hydrocarbons (from combustion of fossil fuels,

wood, cigarettes), terpenes, molds, etc.

Neurotoxicity of Pesticides

Pesticides kill insects by disrupting the

nervous system. The primary action of chlorinated

pesticides – which includes endrin, aldrin,

toxaphene, benzenehexachloride (BHC),

HCH, DDT, heptachlor, heptachlor epoxide,

chlordane, trans-nonachlor, polychlorinates,

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dicofol, chlorobenzilate, mirex, HCB, methoxychlor

and ethylan – is interfering with axonal

transmission by disrupting ion flux, leading

to over-stimulation of the nerves and uncontrolled

neuronal discharge. Symptoms of

acute human toxicity include headache, nausea,

vomiting, hyperesthesias, irritability, confusion,

convulsions, respiratory depression,

cardiac arrhythmia, aplastic anemia, and porphyria

cutanea tarda.

DDT, the best known of this class, was

synthesized in 1874. Its pesticide activity was

found in 1939, and it was used extensively by

the U.S. military in World War II to control

typhus, malaria, and lice. It was put into use

in U.S. agriculture in 1945, and subsequently

banned in 1974 after the uproar caused by

Rachel Carson’s publication of Silent Spring.

In certain individuals DDT has been shown to

cause changes in electromyographic potential

and symptoms of fatigue, poor cognition, withdrawal

from reality, blurred vision, headache,

and ataxia.56,57

Levels of gamma HCH and dieldrin

have been found to be higher in the brain tissue

of persons with Parkinson’s disease than

in controls.58 Elevated levels of DDE were also

found in the substantia nigra in these

Parkinson’s patients. Lindane (gamma HCH)

blocks the chloride ion channel by antagonizing

GABA stimulation of chloride ion uptake

through benzodiazepine receptors.

Lindane can dramatically reduce the

time needed for establishing CNS kindling,

lower the convulsive threshold,

and prolong the sensitivity to convulsive

stimuli even after its clearance

from the blood.59 Having such potential

for increasing seizure activity, it

is surprising Lindane is allowed in

shampoo treatments for head lice in

children and adults.

The OP pesticides were first

synthesized in 1820. These compounds

were developed by Germany

as nerve gases for military use during

World War II. Their present-day nerve gas relatives

include Sarin, recently used in a Japanese

terrorist attack in the Tokyo subway system.

60 They were first used as pesticides in


OP pesticides are rapidly absorbed following

inhalation or ingestion. Dermal absorption

is slower but prolonged exposure can result

in severe poisoning. Once absorbed, OP

compounds accumulate in fat, liver, kidneys,

and salivary glands.61 Instead of affecting axonal

transmission, as chlorinated hydrocarbons

do, they are acetylcholinesterase (AChE) inhibitors

via phosphorylation. This leads to accumulation

of acetylcholine, which binds to

and stimulates muscarinic receptors (found in

autonomic ganglia, CNS, heart, salivary

glands, and smooth muscles) and nicotinic receptors

(autonomic ganglia, skeletal muscle,

and CNS). The brain initially over-stimulates;

later there is paralysis of neural transmission.

Antibodies to the cytochrome P450 hepatic

detoxification system are also generated.

OP toxicity is heightened by the presence

of the solvents toluene and xylene, which

are found in some commercial OP products as

“inert ingredients.” Synergistic toxicity is also

found with OP compounds and polycyclic aromatic

hydrocarbons from auto exhaust.62 The

combination of neurotoxicity of solvents and

Figure 1: Dichlorophenyltrichloroethane (DDT)


Cl Cl


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organophosphates can cause axonal and myelin

degeneration in distal fibers. Their neurotoxic

effect may be more pronounced in older

individuals, partly due to the normal decline

of AChE with aging.63 Neonatal exposure to

both OP and chlorinated pesticides appears to

potentiate the neurotoxic effects if re-exposure

occurs later in life.64

Symptoms of acute organophosphate

poisoning include (1) nausea, vomiting, abdominal

cramps, and diarrhea; (2) salivation

and rhinorrhea; (3) headache and vertigo; (4)

fixed pinpoint pupils, blurred vision, and ocular

pain; (5) muscle twitches (face, tongue, and

neck); (6) difficulty breathing (from excess

secretions); and (7) respiratory paralysis and


The acronym “SLUDGE” – for salivation,

lacrimation, urination, defecation, gastrointestinal

disturbances, and emesis – is often

used for the toxic picture of these compounds.

If the antidote pralidoxime (2-PAM)

is not given within 24-48 hours, the AChEphosphate

bond becomes so strong that physiologic

recovery depends on new synthesis of

AChE. AChE is restored to the affected area

in about two weeks, but in the whole body it

can take up to three months to recover. Serum

testing for red blood cell AChE levels is often

inconclusive except in the most serious poisonings.

One study looked at both central nervous

system effects via SPECT scans and red

blood cell cholinesterase levels. Patients were

differentiated into three groups, latent poisoning,

mild and moderate poisoning, and severe

poisoning. While all groups showed CNS damage

on SPECT scans only the severe poisoning

group had AChE levels below normal.65

Ishikawa has studied organophosphate

poisoning in Japan, and found that in addition

to being neurotoxic, OPs cause severe oxidative

damage and stress, resulting in decreased

selenium concentration in the brain and kidneys

within 14-21 days of exposure.66 He also

found docosahexanoic acid (DHA) (animals

15 mg/kg/day, humans 5mg/kg/day), but not

eicosapentaenoic acid (EPA), crossed the

blood-brain barrier and prevented a rise in superoxide

radicals secondary to OP exposure.

The areas of greatest oxidative damage were

the eyes (including optic nerve atrophy,

neuroretina, and the destruction of retinal pigment),

brain, and heart. Neurological changes

unrelated to AChE inhibition include behavioral

abnormalities, anxiety, irritability, confusion,

depression, and fatigue.

Carbamates are also AChE-inhibiting

pesticides, but they accomplish this by reversible

carbamylation, not phosphorylation.

SLUDGE symptoms can still be present, as

carbamates primarily affect muscarinic and

nicotinic receptors.

Chronic CNS symptoms have been frequently

reported after repeated exposure to OP

and carbamate compounds. Exposed greenhouse

workers exhibited longer reaction times

and reduced motor steadiness as well as increased

tension, depression, and fatigue.67

When matched with controls, workers in a factory

making OP pesticides showed no difference

in AChE levels but did show greater problems

with memory, learning, and vigilance.68

Sheep ranchers exposed to OP compounds in

the course of sheep dipping exhibited poorer

sustained attention and speed of information

processing than non-exposed controls. The

ranchers also showed greater vulnerability to

psychiatric disorders than controls.69

When compared with controls, workers

applying termiticide demonstrated poorer

performance on pegboard turning tests and

postural sway tests. They also displayed significantly

more symptoms of memory disturbances,

altered emotional states, fatigue, and

loss of muscle strength.70 Such neurotoxic effects

can be found years after a single OP poisoning

episode. Thirty-six such individuals

were re-evaluated two years after a single episode

of unintentional OP intoxication. On reexamination

the poisoned group did worse

than the control group on all neuropsychological

subtests, as well as other tests for verbal

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and visual attention, visual memory,

visuomotor speed, sequencing, problem solving,

motor steadiness, and dexterity.71

Animal studies have shown that inutero

exposure to OP compounds result in

impairment on maze performance, locomotion,

and balance in neonates.72

Peripheral neuropathy is also a common

sequelae of OP exposure. South African

farm workers exposed to OP pesticides who

reported significantly more problems with dizziness,

sleepiness, and headache were also

found to have reduced vibratory sense and increase

in hand tremor.73 Flower bulb farmers

were noted to have decreased conduction velocity

of fast and slow motor fibers of the median

and peroneal nerves as well as sensory

fibers of the median and sural nerves.74

Ecuadorian pesticide applicators exhibited

a significantly greater incidence of poor

coordination, abnormal deep tendon reflexes,

and reduced strength than non-exposed local

controls.75 Of 217 chlorpyrifos poisoning incidents

reported by DowElanco, 21 cases had

some evidence of peripheral neuropathy.

Symptoms of delayed neuropathy typically

show up several days to four weeks after

acute organophosphate exposure. Early signs

are paresthesias, weakness and ataxia, gait

changes, or flaccid paralysis. Some of the

chronic neurotoxic effects of OP pesticides

may be due to their ability to induce the formation

of antibodies to neuronal tissues. Antibodies

to myelin basic protein, neurofilament

triplet protein, and glial fibrillary acidic proteins

have all been exhibited after OP exposure.

76 Other antibodies to smooth muscle,

parietal cells, brush borders, and thyroid have

been demonstrated, as well as antinuclear antibodies.


Immunotoxicity of Pesticides

The patient with chronic environmental

pesticide overload generally presents to the

clinician with either the above-mentioned neurotoxic

manifestations or those of

immunotoxicity. Different pesticides can cause

varying effects on the immune system of any

given individual. However, in viewing the

overall effect, toxin exposure causes a specific

immunologic imbalance unseen by other causative

agents, including a general decrease in

cell-mediated immunity (CMI) and an increase

in humoral immune response.79-82 The reduction

in CMI can include reductions or elevations

of T cell counts, including natural killer

cells, depending on the specific compound.83

In general, chemotactic and phagocytic responses

are significantly reduced. Many chlorinated

compounds also cause reduction of

thymic weight and function. Natural killer cell

activity is universally reduced.

These changes result in the clinical

picture of decreased resistance, and an increase

in allergies and certain cancers. The elevation

of humoral immunity often results in production

of antibodies to various tissues, as previously

mentioned,77 and is also seen in exposure

to chlorinated pesticides.84 The

immunotoxic effects can be modulated by several

factors, including level of exposure, nutritional

status (low protein), concurrent pathologic

conditions, biotransformation and activity

of metabolites, physical and emotional

stress, and oxidative stress.85 Both OP and chlorinated

pesticide exposure have been associated

with chronic fatigue syndrome.86,87

One of the most published and contested

arenas of pesticide-induced

immunotoxicity is the area of oncology. Some

studies looking only at DDT exposure and serum

levels have failed to show any significant

increase in cancer mortality or long-term

health effects.88,89 However, when the large

picture of pesticide use is viewed, a positive

correlation with cancers is noted.90 Pesticide

exposure causes DNA damage and the formation

of DNA adducts, which can ultimately

lead to cancer formation.91

OP pesticide use has been associated

with aplastic anemia and leukemia in exposed

farmers,92,93 and in children exposed from


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having their homes treated.94 The studies

involving U.S. farmers and their exposed

children revealed a positive association with

both OP and pyrethroid pesticide exposures

and these hematologic disorders. Increased

rates of multiple myeloma have also been

associated with OP exposure.95 Chlorinated

pesticides are positively associated with the

incidence of non-Hodgkin’s lymphoma,96-98

aplastic anemia,99 cancers of the liver, colon/

rectum, and lung,100,101 multiple myeloma,102

pancreatic cancers,103,104 blood dyscrasias and

leukemia,105 and acute myeloid leukemia

(along with solvent exposure).106,107

The issue of the association of chlorinated

products with breast cancer has been the

subject of numerous studies, and is beyond the

scope of this article. Many studies have found

a positive association between breast cancer

and chlorinated pesticides108-116 and many have

not.117-120 In the positive studies, associations

have been made between breast cancer and

adipose levels of DDT, DDE, PCB, dieldrin,

and HCH.

While this question seems far from

being settled it appears obvious that pesticide

load in some women may be a factor in the

development of breast cancer. A recent study

showed that women with a genetic polymorphic

variant of cytochrome P450-1B1 – which

catalyzes the formation of 4-hydroxyestradiol

that retains significant estrogenic activity and

whose metabolites can generate potentially

mutagenic free radicals that may damage DNA

– have a greatly elevated risk of breast cancer.

121 It was noted that polycyclic aromatic

hydrocarbons and chlorinated pesticides are

all known inducers of CP450. Such an induction,

associated with genetic polymorphism,

might partly explain why pesticides are an

apparent risk factor in some women but not


Endocrine Toxicity from Pesticides

After symptoms appear in the immunological

and neurological realms, problems

in endocrine function may also occur. Such

hormonal imbalances are rarely the first to be

noted when taking a chronological medical

history. Chlorinated products are known to act

as weak estrogens with potential for reproductive

disruption122 and to act as androgen antagonists.

123 These compounds have been associated

with female infertility,124 miscarriages,

125 and possibly male infertility.126 OP

pesticides have also been associated with male

infertility, with increased LH production (possibly

secondary to testicular damage),127 and

reduced numbers of morphologically normal

and live spermatozoa.128

In addition to possibly affecting reproduction,

pesticides can cause other endocrine

problems. HCH, but not DDT, has been shown

to modify pineal synthesis of melatonin.129

DDE, the metabolite of DDT, can accumulate

in the zona fasciculata in the adrenals130 and

lead to adrenal atrophy.131 In animal models

vacuolization and necrosis in the zona

fasciculata secondary to DDE exposure appears

most profound in fetal and neonatal animals,

and less so in adults. The DDT metabolite

also appears to be a tissue-specific toxicant

to the zona fasciculata.132 Reviews on

these and other endocrine effects from environmental

chemicals can be found in the literature.


Other published health effects from

pesticides include renal tubular toxicity from

an OP compound accompanied with elevated

hydrogen peroxide production and increased

lipid peroxidation.135 This again shows the

extensive oxidative damage that OP compounds

can cause. OP compounds have also

been linked to reduced bone formation.136 Agricultural

workers exposed to OP compounds

had significantly decreased bone formation

than healthy controls.

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Clinical Assessment

It should be recognized that all individuals

are exposed to pesticides and that all

carry some level of these toxins in their serum

and adipose tissue. In addition, numerous

variations in genetics, diet, lifestyle, and environment

can interplay to either facilitate or

conspire against clearance of these compounds

from the body. Once a chronological medical

history is obtained, the classic pattern of neurotoxicity

and immunotoxicity, possibly followed

by endocrine toxicity, may be seen.

Once seen or suspected, testing may be warranted.

Because chlorinated compounds are fat

soluble and bioaccumulative they can be easily

measured in serum. This can be done either

fasting or non-fasting, although non-fasting

samples tend to show higher levels.137 Most

authors recommend the lipid content of the

blood be looked at simultaneously so compounds

can be rated as per gram of lipid. This

provides the best correlation with adipose

samples. However, serum and adipose

samples can be vastly divergent.

Table 1 shows the variance between

serum and adipose samples from one individual.

If an adipose sample is to be taken,

it is recommended that adipose tissue be

taken from three different sites, as toxin distribution

is uniform. Laboratories that specialize

in testing these compounds do not

give results in amount of toxin per gram of

lipid as the literature suggests, but in ng/ml

of blood. The laboratories also provide levels

of their laboratory averages as a reference

range. These are the averages of tests

done by the specific laboratory, and do not

necessarily represent “normal ranges” in the

United States.

These laboratories also perform

urine analysis for metabolites of organophosphates

and carbamates. These compounds

are generally cleared from the urinary

tract within 14 days of exposure and

do not show exposure prior to that time. As

mentioned earlier, testing for red blood cell

acetylcholinesterase levels is generally not

definitive except in cases of serious poisoning.

Some laboratories also offer testing for

autoantibodies that can be formed from exposure

to pesticides and solvents. Testing of immune

parameters, including lymphocyte subpopulations

and natural killer cell activity, may

also give an indication of immunotoxicity.

Treatment for Chronic Pesticide


The first step in treating any toxic individual

is avoidance of further exposure. Recognizing

that pesticide use is ubiquitous, this

may not be easy. Avoidance can include consuming

organic foods, avoiding living in or

traveling through agricultural areas during

spraying seasons, avoidance of public buildings

after spraying has taken place, finding out

Table 1: Chlorinated Pesticides in Serum

and Adipose Samples (parts per billion).

Courtesy of Accu Chem Laboratories.

Compound Serum Adipose

HCB <0.3 135

Endrin <0.3 168

Beta-BHC <0.3 1657

Gamma-BHC <0.3 121

Heptachlor <0.3 63

Hep-Epoxide <0.3 33

Oxychlordane 0.4 72

Trans-nonachlor 0.3 123

Dieldrin <0.3 36

DDE 14.2 284

DDT <0.3 222


Alternative Medicine Review _ Volume 5, Number 5 _ 2000 Page 441

Copyright©2001 Thorne Research, Inc. All Rights Reserved. No Reprint Without Written Permission

when neighbors or governmental agencies are

planning to spray an area, etc.

In addition, it should be determined

whether their present dwelling had been termite-

treated (chlordane has a half-life of 20

years) or had other pesticide treatments. Carpeting

from previous owners when the dwelling

was treated would contain pesticide residues,

as would the dust in furnace ducts, both

of which would need to be remediated. The

fewer pesticides personally used, and the fewer

foods or other consumer products purchased

that rely on pesticide use will ultimately reduce

the amount of pesticides released into the


The second treatment step is supplementation

of the nutrients needed to help clear

pesticides from the body, restore common pesticide-

induced deficiencies, and prevent tissue

damage from these compounds. Dietarily,

adequate protein and reduced sugar intake

ensures proper liver clearance of xenobiotics

from the blood. Whey protein increases glutathione

levels in addition to providing complete

protein to the body, which enhances

liver function, making it the first choice for

such cases. Chlorinated pesticides and other

chlorinated compounds reduce the available

vitamin A and thiamine to normal tissues,

the deficiency of which tends to increase the

toxic effect of pesticides.

In addition to these nutrients, a high

quality multiple vitamin/mineral supplement

with extra magnesium, pyridoxine, selenium,

antioxidants, and milk thistle is recommended.

Vitamin C should be taken in

maximal doses to help clear toxins from the

blood and to provide high antioxidant activity.

Docosahexanoic acid (DHA) is necessary

for any OP exposure to increase antioxidant

activity in the brain and prevent OPinduced


If elevated levels of chlorinated pesticides

are found in serum or tissue, additional

measures may be necessary, such as

the frequent use of low temperature saunas,

hydrotherapy, and colonic irrigation.138


Pesticides are ubiquitous in the environment.

Residues of chlorinated pesticides

are present in the air, soil, and water, as well

as in most humans. Organophosphate and carbamate

pesticides—the compounds comprising

the bulk of current pesticide use—are carried

around the globe on air currents. These

pesticides are used in schools, churches, business

offices, apartment buildings, grocery

stores, and homes on a regular basis. Pesticides

are primarily neurotoxins, causing both

acute symptoms as well as chronic effects from

repeated low-dose exposures. These compounds

adversely affect the immune system,

primarily causing cell-mediated immune deficiency,

allergy, and autoimmunity. Multiple

Pesticide Protection and Detoxification.

Avoid Further Exposure

Nutritional Supplementation

Adequate protein (whey preferably)

Decrease sugar intake

Vitamin A

Vitamin B1 (Thiamine)


Vitamin B6 (Pyridoxal 5’-phosphate)



Silybum marianum (milk thistle)

Vitamin C


Adjunctive Therapies

Low-temperature sauna


Colonic irrigation

Page 442 Alternative Medicine Review _ Volume 5, Number 5 _ 2000

Copyright©2001 Thorne Research, Inc. All Rights Reserved. No Reprint Without Written Permission

endocrine effects can alter reproduction and

stress-handling capacity. Laboratory testing to

determine if a toxic pesticide overload exists

is limited to serum pesticide levels and immune

system parameters. Treatment for pesticide

toxicity includes avoidance, nutritional/botanical

supplementation, and detoxification/



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